ArticleThe Journal of physiology2009
Real-time monitoring of cAMP levels in living endothelial cells: thrombin transiently inhibits adenylyl cyclase 6.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Quantifying and mathematical modelling of the influence of soluble adenylate cyclase on cell cycle in human endothelial cells with Bayesian inference.Journal of cellular and molecular medicine · 2022Article
- Physiological roles of mammalian transmembrane adenylyl cyclase isoforms.Physiological reviews · 2022Review
- Real-time monitoring of cAMP in brown adipocytes reveals differential compartmentation of βMolecular metabolism · 2020Article
- Malaysian Tualang Honey Inhibits Hydrogen Peroxide-Induced Endothelial Hyperpermeability.Oxidative medicine and cellular longevity · 2019Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- A Role for Calcium-Activated Adenylate Cyclase and Protein Kinase A in the Lens Src Family Kinase and Na,K-ATPase Response to Hyposmotic Stress.Investigative ophthalmology & visual science · 2017Article
- The Pseudomonas aeruginosa Exoenzyme Y: A Promiscuous Nucleotidyl Cyclase Edema Factor and Virulence Determinant.Handbook of experimental pharmacology · 2017Review
- The ins and outs of adrenergic signaling.Journal of molecular medicine (Berlin, Germany) · 2015Review
- Intracellular Ascorbate Prevents Endothelial Barrier Permeabilization by Thrombin.The Journal of biological chemistry · 2015Article
- Development of FRET biosensors for mammalian and plant systems.Protoplasma · 2014Review
- Adenylyl cyclase 6 mediates loading-induced bone adaptation in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- PKA compartmentalization via AKAP220 and AKAP12 contributes to endothelial barrier regulation.PloS one · 2014Article
- Myosin light chain kinase signaling in endothelial barrier dysfunction.Medicinal research reviews · 2013Review
- Attenuation by sphingosine-1-phosphate of rat microvessel acute permeability response to bradykinin is rapidly reversible.American journal of physiology. Heart and circulatory physiology · 2012Article
- Scanning ion conductance microscopy: a convergent high-resolution technology for multi-parametric analysis of living cardiovascular cells.Journal of the Royal Society, Interface · 2011Review
- Emerging themes of cAMP regulation of the pulmonary endothelial barrier.American journal of physiology. Lung cellular and molecular physiology · 2011Review
- FRET measurements of intracellular cAMP concentrations and cAMP analog permeability in intact cells.Nature protocols · 2011Article
- Temporally resolved cAMP monitoring in endothelial cells uncovers a thrombin-induced [cAMP] elevation mediated via the Ca²+-dependent production of prostacyclin.The Journal of physiology · 2011Article
- Rapid calcium-dependent reduction of intraendothelial cAMP: a trigger to increase vascular permeability?The Journal of physiology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The crosstalk between Ca(2+) and cAMP signals plays a significant role for the regulation of the endothelial barrier function. The Ca(2+)-elevating agent thrombin was demonstrated to increase endothelial permeability and to decrease cAMP levels. Since Ca(2+) and cAMP signals are highly dynamic, we aimed to study the temporal resolution between thrombin-evoked Ca(2+) signals and subsequent changes of cAMP levels. Here we conduct the first real-time monitoring of thrombin-mediated regulation of cAMP signals in intact human umbilical vein endothelial cells (HUVECs) by utilising the Ca(2+)-sensitive dye Fluo-4 and the fluorescence resonance energy transfer (FRET)-based cAMP sensor Epac1-camps. We calibrated in vitro FRET responses of Epac1-camps to [cAMP] in order to estimate changes in intracellular [cAMP] evoked by thrombin treatment of HUVECs. After increasing [cAMP] to 1.2 +/- 0.2 microm by stimulation of HUVECs with isoproterenol (isoprenaline), we observed a transient decrease of cAMP levels by 0.4 +/- 0.1 microm which reached a minimum value 30 s after thrombin application and 15 s after the thrombin-evoked Ca(2+) peak. This transient decrease in [cAMP] was Ca(2+)-dependent and independent of a G(i)-mediated inhibition of adenylyl cyclases (ACs). Instead the knock down of the predominant subtype AC6 in HUVECs provided the first direct evidence that the Ca(2+)-mediated inhibition of AC6 accounts for the thrombin-induced decrease in cAMP levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.